The many roads traveled by Helicobacter pylori to NFκB activation
The many roads traveled by Helicobacter pylori to NFκB activation
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DOI：
10.4161/gmic.1.2.11587
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发表时间：
2010-01-01
期刊：
影响因子：
12.2
通讯作者：
Chen, Lin-Feng
中科院分区：
文献类型：
--
作者：
Lamb, Acacia;Chen, Lin-Feng
许多与幽门螺杆菌相关的病症是由细菌在宿主胃中诱发慢性炎症的能力引起的。调节炎症的主要转录因子之一是 NF kappa B，它在包括某些胃癌在内的许多癌症中持续激活。幽门螺杆菌已被证明可以使用几种不同的细菌成分和宿主信号通路以细胞类型和菌株特异性的方式激活 NF kappa B。我们最近的研究表明，H. pylori 利用其毒力因子 CagA 靶向信号分子 TAK1 来激活 NF kappa B。在本文中，我们将总结我们的发现以及 H. pylori 介导的 NF kappa B 激活的其他最新进展，并讨论 CagA 和 TAK1 在 H. pylori 介导的 NF kappa B 激活和胃疾病中的作用。
Many of the pathologies linked to Helicobacter pylori are caused by the ability of the bacteria to induce chronic inflammation in the stomach of the host. One of the major transcription factors that regulate inflammation is NF kappa B, which is constitutively activated in many cancers including some gastric cancers. H. pylori has been shown to activate NF kappa B using several different bacterial components and host signaling pathways in cell-type and strain-specific ways. Our recent studies demonstrate that H. pylori utilizes its virulence factor CagA to target signaling molecule TAK1 for the activation of NF kappa B. In this article, we will summarize our findings together with other recent progress in the H. pylori-mediated activation of NF kappa B and discuss the role of CagA and TAK1 in the H. pylori-mediated activation of NF kappa B and gastric diseases.